Retinitis pigmentosa (RP) is the name given to a group of inherited eye diseases that affect the retina (the light-sensitive part of the eye). RP causes the breakdown of photoreceptor cells (cells in the retina that detect light).
Photoreceptor cells capture and process light helping us to see. As these cells breakdown and die, patients experience progressive vision loss.
The most common feature of all forms of RP is a gradual breakdown of rods (retinal cells that detect dim light) and cones (retinal cells that detect light and color). Most forms of RP first cause the breakdown of rod cells. These forms of RP, sometimes called rod-cone dystrophy, usually begin with night blindness. Night blindness is somewhat like the experience normally sighted individuals encounter when entering a dark movie theatre on a bright, sunny day. However, patients with RP cannot adjust well to dark and dimly lit environments.
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As the disease progresses and more rod cells breakdown, patients lose their peripheral vision (tunnel vision). Individuals with RP often experience a ring of vision loss in their periphery, but retain clear central vision. Others report the sensation of tunnel vision, as though they see the world through a straw. Many patients with retinitis pigmentosa retain a small degree of central vision throughout their life.
Other forms of RP, sometimes called cone-rod dystrophy, first affect central vision. Patients first experience a loss of central vision that cannot be corrected with glasses or contact lenses. With the loss of cone cells also comes disturbances in color perception. As the disease progresses, rod cells degenerate causing night blindness and peripheral vision.
Symptoms of RP are most often recognized in children, adolescents and young adults, with progression of the disease continuing throughout the individual’s life. The pattern and degree of visual loss are variable.
Retinitis pigmentosa is an inherited disorder, and therefore not caused by injury, infection or any other external or environmental factors. People suffering from RP are born with the disorder already programmed into their cells. Doctors can see the first signs of retinitis pigmentosa in affected children as early as age 10. Research suggests that several different types of gene mutations (changes in genes) can send faulty messages to the retinal cells which leads to their progressive degeneration. In most cases, the disorder is linked to a recessive gene, a gene that must be inherited from both parents in order to cause the disease. But dominant genes and genes on the X chromosome also have been linked to retinitis pigmentosa. In these cases, only one parent has passed the disease gene. In some cases, a new mutation causes the disease to occur in a person who does not have a family history of the disease. The disorder also can show up as part of other syndromes, such as Bassen-Kornzweig disease or Kearns-Sayre syndrome.
The below factors can also contribute to your Glaucoma progression.
Neuroprotection therapy helps protect neurons in your eye from injury such as from eye pressure elevations. Neurotrophins helps to provide the required neuroprotective therapy which prevents from death of the ganglion cells in your eyes.
Vascular dysregulation means that blood flow is not properly flowing. This causes reduced and unstable oxygen supply to the tissues in the eyes. This in turn causes a cacade of events causing glaucomatous optic neuropathy.
Oxidative stress damage is an important factor in development of glaucoma, which triggers trabecular meshwork degeneration, which then leads to intraocular hypertension. Different studies provide cumulating evidence, which supports the association of oxidative stress with different aspects of the neurodegenerative process happening in glaucoma.
Glaucoma is associated with toxic inflammatory factors leading to cell death and disease progression. Trabecular meshwork dysfunction is likely mediated by oxidative stress and inflammatory responses. Ocular surface inflammation may compromise the cornea, conjunctiva and the trabecular meshwork.
Excitotoxicity is increased levels of glutamate and is seen in Glaucoma patients which cause
retinal ganglion cell (RGC) death. If the toxic effects of glutamate aren't blocked, RGC loss can continue, leading to further visual impairment.
Netra Restoration Therapy provides the following benefits for patients with Glaucoma.
The level of loss of nerve fiber layer and optic nerve atrophy will determine the level of the improvement seen.
Most patients start to see subjective improvements in their vision within just 7 days of starting the NRT treatment.
NRT treatment can stop Glaucoma vision loss progression or considerably reduced to preserve the remaining vision.
NRT treatment improves visual field by reinstating dormant and sub-optimally functioning retinal cells. Without treatment these cells would eventually neurodegenerate and be lost forever.
With NRT treatment most glaucoma patients have shown improvement in their visual acuity by a minimum of 1 to 2 lines in distant and near vision.
Most glaucoma patients treated with NRT treatment have shown marked improvement in their color contrast.
Most glaucoma patients treated with NRT treatment have experienced having brighter vision, a reduction in glare, and blurry/cloudy vision.